The purpose of the present study is to determine if bethanechol and/or xenin-25 increase postprandial cholinergic input to islets and if this signaling is associated with changes in postprandial glucose, GIP, GLP-1, insulin, C-peptide, glucagon, and PP levels and insulin secretion rates (ISRs) in humans with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) and T2DM. The gene discussed is GCG; the disease is Impaired glucose tolerance.